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Flashcards in Applied Anatomy of the Heart Deck (44)

Describe the cardiac plexus

This plexus lies anterior to the tracheal bifurcation and just posterior to the arch of the aorta. It contains parasympathetic fibres from the vagus nerve, sympathetic fibres from the sympathetic trunk and visceral general afferents


How do the neurones of the parasympathetic nervous system differ from those of the sympathetic nervous system?

Parasympathetic: long pre-ganglionic fibres and short post-ganglionic fibres

Sympathetic: short-preganglionic fibres and long post-ganglionic fibres


Describe the parasympathetic innervation to the heart

Parasympathetic supply is from the vagus nerve and it reduces the heart rate by acting on the SAN and AVN. This is stimulated by the cardio-inhibitory centre in the medullary reticular formation.


Describe the sympathetic innervation to the heart

Sympathetic neurones from the thoracic trunk (T1-T4) contribute to the cardiac plexus and synapse with the SAN, AVN and coronary vascular smooth muscle to increase heart rate and contractility (positive inotropic and chronotropic effects). This is mediated by the cardio-accelerators centre in the medullary reticular formation


Explain why you get cardiac referred pain in ischaemia

In regions of ischaemia the lactate build up stimulates nociceptors in the myocardium which stimulate the visceral general afferent fibres. These VGAs then ascend through the cardiac branches of the sympathetic trunk (T1-T4 mainly) and therefore this pain is referred to these dermatomes (medial-upper arm, shoulder and jaw) - this is seen in angina


Why may you get cardiac referred pain to the epigastric region?

If there is an inferior myocardial infarction then this will stimulate nociceptors which will stimulate VGAs which travel in the T5-T9 sympathetic fibres and therefore the supplied dermatomes are in the epigastric region


Why is the left anterior descending artery known as the 'widow maker'?

The bundle branches (Hiss bundles) in the interventricular septum are predominantly supplied by the left posterior descending artery (branch of LAD) and therefore if there is a loss of blood supply from this artery, due to an occlusion, then this will prevent the conduction of electrical impulses down the bundles of Hiss and therefore prevent ventricular contraction, which can lead to heart failure and death.


What does it mean whether someone is left or right-dominant in the context of coronary arterial supply?

This is determined by which coronary artery supplies the AV nodal branch of the posterior descending/interventricular artery. This is usually supplied by the right coronary artery (70%) and this is known as right-dominance. If the AV nodal branch is supplied by the left circumflex this is left-dominance (10% of the time), but the AV nodal branch may be supplied by both the RCA and LCA and this is known as co-dominance (20% of the time)


What is 'cardiac remodelling'?

Increase in myocardial mass


What are physiologic causes of cardiac remodelling?

Pregnancy and athleticism


What are pathologic causes of cardiac remodelling?

> Pressure overload (increased afterload) - seen in hypertension and aortic stenosis (as increased pressure is needed to overcome narrowing)

> Volume overload (increased preload) - e.g. if there is valvular regurgitation or hypervolaemia

> Cadiac injury - damage can lead to reduced contractility of affected portion due to fibrous scar formation and wall thinning, therefore compensatory hypertrophy may occur to facilitate the same strength of contraction


What is concentric ventricular hypertrophy?

Wall thickness of the ventricles increases (due to production of new sarcomeres added in parallel) and therefore the wall becomes stiffer (less compliant) so ventricular filling is compromised.

This form of hypertrophy occurs due to an increase in after load (pressure) as seen in aortic stenosis or chronic hypertension.


What is eccentric ventricular hypertrophy?

New myofibrils/sarcomeres are added in series (side-by-side) and therefore the ventricular wall doesn't thicken but the size of the heart itself increases; contractility is reduced, cardiac oxygen demand increases and there is less mechanical efficacy.

This occurs due to volume overload (increased preload) as seen in aortic/mitral regurgitation and hypervolaemia


What's the difference between eccentric and concentric ventricular hypertrophy?

Concentric hypertrophy leads to wall thickening whereas eccentric hypertrophy leads to overall cardiac enlargement (due to myofibril deposition in series)


Explain what is meant by bundle branch block.

Where there is ischaemia in one of the blood vessels which supplies the bundle of Hiss in the septum and therefore conduction from the AVN has to travel down the myocardium of the ventricular walls which slows the impulse speed (lengthens QRS) and leads to loss of ventricular synchrony


What are the signs of bundle branch block?

Elongated QRS complex (due to propagation down the myocardium instead of the bundles, which takes longer) and loss of ventricular synchrony


Explain what is meant by atrial fibrillation

Where many sites in the atrium begin producing electrical impulses other than the SAN which overwhelms the AVN and leads to uncoordinated ventricular contraction


What are the signs and symptoms of atrial fibrillation?

There are absent p-waves (too many random, uncoordinated atrial depolarisations to produce a single peak), tachycardia and reduced cardiac output (can lead to thrombi formation)


What does the first heart sound (S1/'lubb') represent?

Lubb is the closing of the mitral and triscuspid valves (marking the beginning of systole)


What does the second heart sound (S2/'dubb') represent?

Dubb is the closing of the aortic and pulmonary valves (marking the beginning of diastole)


What are the common causes of valvular disease?

Inflammation (as seen with infection), ageing, cardiomyopathy, IHD, fibrosis and calcification (seen in ageing), stenosis of the valves, and valvular incompetence.


How can rheumatic disease lead to valvular disease?

The valve cusps fibrose, but the cordae tendinae also soften.


What are the four main types of valvular dysfunction?

Mitral regurgitation, mitral stenosis, aortic regurgitation, aortic stenosis


What is mitral (valve) regurgitation?

This is the most common valvular dysfunction and it involves the back flow of blood into the left atrium during ventricular systole which causes acute volume overload


What causes mitral (valve) regurgitation?

Mitral valve prolapse and rheumatic heart disease


What are the consequences of (mitral) valve regurgitation?

The increased preload and chronic mitral regurgitation may lead to left atrial enlargement (thickened wall) and left ventricular hypertrophy (eccentric, dilated chamber).


What is aortic (valve) stenosis?

Narrowing of the aortic valve


What are the consequences of aortic (valve) stenosis?

The left ventricle has to compensate for this narrowing by generating an increased pressure to overcome this, leading to concentric ventricular hypertrophy. This ventricular hypertrophy leads to a reduced compliance and a decreased reserve of coronary blood flow.


What is aortic (valve) regurgitation?

When there is blood back flow into the ventricle following ventricular contraction


What is the cause of aortic (valve) regurgitation?

Occurs when there is a chronic volume overload which leads to stretching and elongation of the myocardial fibres in the ventricles


What are the consequences of aortic (valve) regurgitation?

As a result of the increased pre-load and ventricular stretching, the left ventricle undergoes eccentric hypertrophy (enlarges but thins) and this leads to left ventricular dilatation which can lead to congestive heart failure as a result of the decreased cardiac output.


What is mitral (valve) stenosis?

Narrowing of the mitral valve and therefore the left atrium is responsible for producing a greater pressure to overcome the impingement


What are the consequences of mitral (valve) stenosis?

As the ‘atrial kick’ has to be stronger, this results in atrial enlargement and increased atrial pressure. In addition, the stenosis restricts the amount of ventricular filling possible in diastole, and subsequently the cardiac output is reduced. If the left atrium enlarges too much it can lead to atrial fibrillation


How would mitral regurgitation present on chest auscultation?

Mitral regurgitation would be heard as a pan-systolic murmur (after S1)


How would aortic stenosis present on chest auscultation?

Aortic stenosis would be heard as a mid-systolic murmur (after S1)


How would aortic regurgitation present on chest auscultation?

Aortic regurgitation would be heard as a pan-diastolic murmur (after S2)


How would mitral stenosis present on chest auscultation?

Mitral stenosis would be heard as a mid-diastolic murmur (after S2)


How can cardiac dysfunction lead to pulmonary oedema?

If there is a failure of the left side of the heart, this leads to an increases pressure at the venous end of the capillaries in the pulmonary circuit (pulmonary venous hypertension). This is because prior to the failure region (which will likely be coagulating) the pressure will subsequently rise, and therefore if there is right heart failure, there is systemic oedema, whereas the oedema is pulmonary if there is left heart failure.


Which ECG leads provide an image of the lateral heart? What coronary arteries supply this region?

V5, V6, aVL and I; supplied by the branch of the LAD or left circumflex artery


Which ECG leads provide an image of the anterior heart? What coronary arteries supply this region?

V3, V4; supplied by the left anterior descending (LAD) artery


Which ECG leads provide an image of the septal heart? What coronary arteries supply this region?

V1, V2; supplied by the LAD artery


Which ECG leads provide a image of the inferior of the heart? What coronary arteries supply this region?

II, III and aVF; supplied by the right coronary artery or the left circumflex


Where is the AVN located?

In the right atrium


What happens in cardiac remodelling/ventricular hypertrophy?

New sarcomeres are formed, there is an increased amount of fibrous tissue, there is a decreased ratio of capillaries to myocytes as well as the synthesis of abnormal proteins and the loss of myocytes. This is likely due to the heart becoming more fibrous than muscular in sites of damage